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    PULMONARY REHABILITATION

    Upper Respiratory TractThe structures of the upper respiratory tract are the nasal cavity, pharynx, and larynx. As air is brought

    into the body, the nasal cavityand pharynx filter and remove

    particles in the air and begin tohumidify and warm it to body

    temperature. The larynx, which

    extends from C3 to C6, controlsairflow; and when it contracts

    rapidly, the epiglottis prevents

    food, liquids, or foreign objectsfrom entering the airway

    Lower Respiratory Tract

    The lower respiratory tract iscomposed of conducting airways

    of the tracheobronchial tree and

    the terminal respiratory units.There are approximately 23

    generations (branchings) of the

    structures within the tracheobronchial tree, which extends from the trachea to the terminal respiratory

    units of the lungs.The first 16 airway branchings of the lower respiratory tract primarily conduct air, whereas the last 6 are

    respiratory airways that end (in the mature lung) in approximately 300 million alveoli. The diameter

    of the airways becomes increasingly smaller with each successive generation of the tracheobronchial tree.

    The trachea is an oval, flexible tube supported bysemicircular rings of cartilage. It extends from C6 inan oblique, downward direction to the sternal angle level

    of rib 2 and T6, at which point it bifurcates into two

    mainstream bronchi: the right, which is directed almost

    vertically, and the left, which is directed more obliquely.The two mainstem bronchi then divide into five lobar

    bronchi: three on the right and two on the left. Mainstem

    and lobar bronchi have a great amount of cartilage,which helps maintain airway patency.

    Each of the lobar bronchi divide into two or more

    segmental bronchi: 10 on the right and 8 on the left.Segmental bronchi have scattered cartilage, smooth

    muscle, elastic fibers, and a capillary network. The

    mainstem, lobar, and segmental bronchi have a mucous

    membrane essentially the same as the trachea.Segmental bronchi divide into subsegmental bronchi and

    bronchioles, which have less and less cartilage

    and ciliated epithelial cells. These bronchioles divide into the terminal bronchioles, which are distal to thelast cartilage of the tracheobronchial tree. Terminal bronchioles contain no ciliated cells. Terminal

    bronchioles divide into respiratory bronchioles and provide a transitional zone between the bronchioles

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    and alveoli. These respiratory bronchioles divide into alveolar ducts and alveolar sacs. One duct may

    supply several sacs. The ducts contain smooth muscle, which narrows the lumen of the duct withcontraction. The alveoli are located in the periphery of the alveolar ducts and sacs and are in contact with

    capillaries (alveolar-arterial membrane). Gas exchange occurs here.

    The lungs are elastic structures, containing collagen and elastic fibers that resist expansion. For normallungs to contain air, they must be distended either by a positive internal pressurei.e., by a pressure in

    the airways and alveolar spacesor by a negative external pressurei.e., by a pressure outside the lung.Ventilation is the process whereby the lungs replenish the gas in the alveoli. Measurements of ventilatory

    function in common diagnostic use consist of quantification of the gas volume contained in the lungs

    under certain circumstances and the rate at which gas can be expelled from the lungs. Because the variouslung volumes and capacities are often abnormal in people with pulmonary disorders, they are routinely

    measured in such patients. The original clinical measuring device, a spirometer, was a simple instrument

    utilizing a hollow bell inverted over water. Now patients simply blow into a small electronic measuring

    device. Spirometry is most useful for evaluating losses in respiratory function and for following thecourse of certain respiratory diseases.

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    Although it cannot provide a specific diagnosis, it can distinguish between obstructive pulmonary disease

    involving increased airway resistance (such as chronic bronchitis) and restrictive disorders involving areduction in total lung capacity resulting from structural or functional changes in the lungs (due to

    diseases such as tuberculosis, or to fibrosis due to exposure to certain environmental agents such as

    asbestos). Increases in TLC, FRC, and RV may occur as a result of hyperinflation of the lungs in

    obstructive disease, whereas VC, TLC, FRC, and RV are reduced in restrictive diseases, which limit lung

    expansion.

    Two other useful tests are FVC and FEV. FVC, or forced vital capacity, measures the amount of gasexpelled when a subject takes a deep breath and then forcefully exhales maximally and as rapidly as

    possible. FEV, or forced expiratory volume, determines the amount of air expelled during specific timeintervals of the FVC test. For example, the volume exhaled during the first second is FEV 1. Those with

    healthy lungs can exhale about 80% of the FVC within 1 second. Those with obstructive pulmonary

    disease exhale considerably less than 80% of the FVC within 1 second, while those with restrictive

    disease can exhale 80% or more of FVC in 1 second even though their FVC is reduced.

    CHRONIC OBSTRUCTIVE PULMONARY DISEASE

    Chronic obstructive pulmonary diseases (COPD) are diseases of the respiratory tract that produce anobstruction to airflow and that ultimately can affect both mechanical function and gas exchangingcapacity of the lungs.

    COPD is also known as chronic obstructive airway disease (COAD) and chronic obstructive lung disease(COLD)

    Certain physical symptoms are characteristic of COPD. This includes:

    Chronic cough Expectoration of mucus Wheezing

    Dyspnea on exertion

    EPIDEMIOLOGY

    COPD is the fourth leading cause of death and affects >16 million persons in the United States.COPD is also a disease of increasing public health importance around the world. Global Initiative for

    Chronic Obstructive Lung Disease (GOLD) estimates suggest that COPD will rise from the sixth to the

    third most common cause of death worldwide by 2020.

    ETIOLOGY

    Genetic predisposition Environmental factors ( allergic diseases , e.g. asthma) Respiratory infections (e.g. bronchopneumonitis) Chemical inflammation (e.g. cigarette smoke, asbestosis) Metabolic abnormalities (e.g. alpha 1-antitypsin def) Cigarette smoking (main cause: chronic bronchitis, emphysema) Smokers are 3.5-25 times more likely (depending on amounts smoked) to die of COPD than non-

    smokers

    PATHOPHYSIOLOGY

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    Changes Associated with Obstructive Lung Diseases:

    Narrowing & obstruction of airways Inflammation of the airways Destruction of alveolar & bronchial walls Increased production & retention of mucus Abnormal pulmonary function tests:

    - decreased vital capacity & expiratory reserve volume- increased residual volume- decreased expiratory flow rates Asthma

    EARLY OBSTRUCTIVE LUNG CONDITION

    BRONCHOPULMONARY DYSPLASIA

    Bronchopulmonary dysplasia is a chronic lung disease of infancy, characterized by respiratory distressand oxygen dependency lasting beyond 1 month of age; that follows the use of oxygen and ventilatory

    support to treat neonatal respiratory distress.

    Etiology

    Barotrauma(injury due to pressure) Intubated infants High oxygen concentration(oxygen toxicity) Pulmonary interstitial edema Infection Congestive heart failure

    Clinical manifestations

    Mild BPD

    Transient tachypnea Cyanosis with feeding or crying

    Severe BPD

    Tachypnea Cyanosis on room air Suprasternal, intercostals and subcostal retractions Nasal flaring Grunting Pulmonary HPN R sided heart failure

    Pathophysiology

    Partial expiratory flow volume (PEFV) reveals low forced expiratory rates Generally decreased lung compliance and functional residual capacity @ early stages

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    Persistent ventilation-perfusion mismatching results in hypoxemia and need for long-term oxygentherapy and possible ventilator support

    Ground-glass appearance is seen on xrays indicating hyaline membrane diseaseCYSTIC FIBROSIS

    Cystic fibrosis is a genetic disorder characterized by dysfunction of the exocrine glands with abnormalsecretions in the respiratory tract, sweat glands, mucosal glands of the small intestine, the pancreas, and

    bile ducts of the liver. Abnormally think, tenacious mucus along with impaired mucociliary clearance

    results in COPD and frequent respiratory infections.

    Etiology

    Cystic fibrosis is an autosomal recessive genetic disease caused by mutations in the gene (long arm ofchromosome 7) encoding the cystic fibrosis transmembrane conductance regulator (CFTR).

    Pathophysiology

    An acute inflammatory/allergic process produces hyperreactive airways and chronic inflammation of

    airways which results in increased V/Q mismatching ad therefore increased work of breathing

    Clinical manifestations

    children with CF usually small for their age due to pancreatic malfunction leading to food mal-absorption.

    exocrine gland dysfunction within pulmonary. increased production of viscous mucus. airwayobstruction. .Chronic airway obstruction + pooling of secretions: vulnerable to pulmonary

    infection.

    Manifests as chronic productive cough; dyspnea, tachypnea; cyanosis. Clinical hallmark: chronic coughing & production of copious amount of thick, purulent mucus PFT show decrease expiratory flow rates; increase residual volume over time (due to

    hyperinflation of the lungs) Average patient survives into the late 20s or early 30s. Pulmonary complications eventually the

    cause of death.

    Cystic fibrosis Triad

    Chronic pulmonary disease Pancreatic deficiency Abnormal high levels of sweat electrolytes: increased NaCl content

    ASTHMA

    Asthma is a chronic inflammatory disease of the airways characterized by increased responsiveness of the

    tracheobronchial tree to a variety of stimuli. Widespread narrowing of the airways occurs when the

    individual comes in contact with these stimuli. Generally asthma is episodic in nature, with acute episodesbeing separated by symptom-free time periods.

    Asthma that begins in childhood as is triggered by allergens is called extrinsic asthma. Asthma that begins

    after age 35 is called intrinsic asthma and is more severe in nature.

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    Etiology

    Allergens Exercise Infections Occupational stress Environmental stress Pharmacologic stress Emotional stress

    Pathophysiology

    Predominant feature seen in PFT: obstruction to airflow, either episodic or continual with varyingseverity

    o Decreased FEV1 and FEV1:FVCo Decreased VCo Increased FRC and RV

    Hyperreactivity of airways to various stimuli results in bronchial smooth muscle contraction andhypertrophy, inflammation of the mucosa and overproduction of viscous, tenacious mucus.

    Severity of airway obstruction may be no uniform in the lungs so that distribution of ventilation isuneven

    o Initially perfusion is diverted away from underventilatedo If obstruction becomes widespread and severe, ventilation-perfusion mismatching

    worsens and arterial hypoxemia occurs

    Clinical manifestations

    intermittent wheezing and dyspnea cough respiratory distress hyperinflated chest, hyperresonant to percussion auscultation reveals prolonged expiratory phase status asthmaticus

    o patients with a severe persistent attack of asthma that is refractory to bronchodilatorso usually in severe respiratory distress and have cyanosiso become physically exhausted by the increased work of breathing and from sleep

    deprivation

    BRONCHIECTASIS

    Bronchiectasis is a permanent, abnormal dilation and distortion of one or more bronchi that is caused bydestruction of the elastic and muscular components of the bronchia walls.

    Etiology

    Necrotizing infection or a series of multiple infections involving the tracheonbronchial walls andadjacent lung parenchyma

    Bacterial pneumoniaso S. aureuso Klebsiella pneumoniao P. aeruginosa

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    Bronchial obstruction Mucoid impaction

    Pathophysiology

    Bronchial obstruction produces atelectasis which increases the intrathoracic pressure required toovercome greater elastic resistance and causes dilation of the bronchi.

    Prolonged bronchial obstruction increases the risk of secondary infection which results indestruction of the bronchial walls and dilation of the bronchi leading to reparative laying down ofthe fibrous tissue.

    Arterial hypoxemia may develop due to ventilation-perfusion mismatching Extensive pulmonary anastomoses occur at precapillary level in the granulation tissue

    surrounding bronchiectatic segments. These can lead to bronchial artery enlargement and left to

    right shunts (recirculation of oxygenated blood).

    Clinical manifestations

    Cough Copious mucopurulent sputum and fetid (having disagreeable odor)

    o Separates into three layers in standingcharacteristic of the disease Upper layer of white/slightly greenish brown frothy secretions Middle thin mucoid layer Bottom layer of thick greenish plugs

    Recurrent pulmonary infections Recurrent hemoptysis Abnormalities on auscultation

    o Moist rales/crackles over involved lobeso Rhonchi during mucus retentiono

    Dullness to percussion and decreased breath sounds during mucus plugging

    ADULT OBSTRUCTIVE LUNG CONDITIONS

    CHRONIC BRONCHITIS

    Chronic bronchitis is characterized by excessive mucus production in the bronchial tree with a chronic orrecurrent productive cough that lasts at least 3 months and recurs over at least 2 consecutive years.

    Hypersecretion begins in the large airways and is not associated with airway obstruction (simple

    bronchitis). Later, hypersecretion progresses to the smaller airways where the airway obstruction beginsinitially (chronic bronchitis)

    Etiology

    Cigarette smoking Air pollution Second-hand smoke Occupational exposure to dusts, such as gold, coal, fluorspar and asbestos Occupational exposure to vegetable dusts, such as cotton, flax or hemp

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    Pathophysiology

    Initially, there is respiratory bronchiolitis with inflammatory and obliterative changes that havebeen initiated by inhaled irritants.

    Small airway disease may not be detectableClinical manifestations

    Chronic productive cough with morning expectoration and clearing of secretions accumulatedduring the night

    Sputum is usually clear and mucoid but can become purulent during the presence of infection. Recurrent chest infections Overweight with a cyanotic cast to their lips and nailbeds; blue bloater Rhonchi and wheezes are frequently heard Prolonged expiratory phase

    EMPHYSEMA

    Emphysema, an alveolar or parenchymal disease, is an abnormal and a permanent enlargement of the air

    spaces distal to the terminal nonrespiratory bronchioles, accompanied by destructive changes of thealveolar walls. Disturbances in lung function result from these anatomic changes, including loss of elastic

    recoil, excessive collapse of airways on exhalation and chronic airflow obstruction.

    4 basic types:

    1. Centrilobular emphysema (CLE) Alveoli arising from the respiratory bronchiole or the proximal portion of the acinus are most

    affected

    Normal alveolar ducts and alveolar sacs No respiratory disability

    2. Panlobular emphysema (PLE)

    All alveoli within acinus are affected to the same degree A nearly uniform destruction f most of the structures within a lobule is seen associated with alpha antitrypsin deficiency and unilateral hyperlucent lung syndrome

    o A.antitrypsin, enzyme produced in the liver inactivates elastase, which if uncheckeddestroys lung elastic tissue

    3. Paraseptal emphysema Enlarged air spaces are at the periphery of the acinus, just under the pleura or along connective

    tissue septa

    These thin-walled, inflated areas located at the pleural surface may become bullae4. Irregular emphysema

    Located in the vicinity of scars and is related to the effects of scarring and contractionEtiology

    Cigarette smoking Environmental air pollution Hereditary deficiency of alpha1-antitrypsin

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    Pathophysiology

    Repeated inflammation of the airways along with the development of partial or complete bronchiolar

    bronchiolar obstruction results in:

    Air trapping and alveolar overdistention which causes fragmentation of the intraalveolar elastictissue and rupture of the attenuated interalveolar septa, leads to coalescence of several alveoli andbullae formation.

    Release of proteases which causes progressive lung destruction Loss of functional alveoli results in gross V/Q mismatching throughout the lungs which increases

    the work of breathing and creates potential for ventilatory muscle fatigue.

    Also increased V/Q mismatching produces increased hypoxemia and possibly CO2 retentionresulting in increased RR and use of accessory muscles and even greater work of breathing.

    Loss of large portions of lung parenchyma decreases the number of pulmonary capillaries whichleads to increased pulmonary hypertension.

    Clinical manifestations

    Shortness of breath Scant sputum production Barrel-shaped configuration of chest wall with increased subcostal angle Hypertrophied accessory muscles of respiration Pursed-lip breathing even at rest Shoulders frequently rounded Thin, sometimes cachectic in body build with rosy skin tones; pink puffer

    DIFFERENTIAL DIAGNOSIS

    Diagnosis Suggestive features

    COPD Mid-life onsetSlowly progressing symptoms

    Long history of smoking

    Asthma Early onset

    Varying symptomsSymptoms during the night/early morning

    Presence of allergy, rhinitis and/or eczema

    A family historyAirflow limitation that is largely reversible

    Congestive heart

    failure

    Fine basilar crackles on auscultation

    Dilated heart on chest radiography

    Pulmonary oedema

    Volume restriction not airflow limitation on pulmonary function tests

    Bronchiectasis Large volume of purulent sputum

    Commonly associated with bacterial infection

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    Coarse crackles/clubbing on auscultation

    Bronchial dilation and bronchial wall thickening on chest radiography/CT

    Tuberculosis Onset at all ages

    Lung infiltrate on chest radiography

    Microbiological confirmationHigh local prevalence of tuberculosis

    Obliterative

    bronchiolitis

    Younger onset and in non-smokers

    History of rheumatoid arthritis/fume exposure?Hypodense areas on expiration on CT

    Diffuse

    panbronchiolitis

    Effects mostly male nonsmokers

    Almost all have chronic sinusitis

    Diffuse small centrilobular nodular opacities and hyperinflation on chestradiography and HRCT

    CT: computed tomography; HRCT: high-resolution computed tomography.

    GENERAL MEDICAL MANAGEMENT

    Pharmacologic therapyo vaccination against influenza and pneumococcal pneumoniao inhaled quaternary anticholinergico b20adrenergic agonist bronchodilatorso inhaled corticosteroidso oral theophylline can improve respiratory muscle endurance

    exposure to environmental and occupational pollution must be prevented 1-antitrypsin augmentation therapy in those with emphysema smoking cessation noninvasive mechanical ventilation lung volume reduction surgery combined long-acting -agonists with inhaled corticosteroids oxygen therapy

    PT GOALS

    Decrease amount and viscosity of secretions and prevent respiratory infections. Remove or prevent accumulation of secretions. Promote relaxation of accessory muscles of inspiration. Improve patients breathing pattern and ventilation. Minimize or prevent episodes of dyspnea. Improve mobility and lower thorax as well as posture. Increase exercise tolerance. Improve overall fitness.

    PT MANAGEMENT

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    Breathing exercises and ventilatory training are fundamental interventions for the prevention orcomprehensive management of impairments related to acute or chronic pulmonary disorders. It

    increases the effectiveness of the cough mechanism, improves strength endurance andcoordination of the muscles of ventilation , correct inefficient/abnormal breathing patterns and

    decrease the work of breathing, relieves dyspnea during exertion among others.

    o Diaphragmatic breathing Patients with primary or secondary pulmonary dysfunction can be taught how to

    control breathing by optimal use of the diaphragm and decreased use of

    accessory muscles.

    Improve efficiency of ventilation Decrease work of breathing Increase the excursion of the diaphragm Improve gas exchange and oxygenation

    o Segmental breathing Teach patient how to expand localized areas of lungs while keeping other areas

    quiet.

    Done during postural drainage or following thoracic surgery when it is importantto emphasize expansion of problem areas of lungs and chest wall

    o Inspiratory resistance training Uses pressure- or flow-based devices to provide resistance to airflow Designed to improve the strength and endurance of muscles of inspiration and

    decrease the occurrence of inspiratory muscle fatigue

    o Incentive spirometry Form of ventilatory training that emphasizes sustained maximum inspirations

    using a small hand-held spirometer that provides visual/auditory feedback about

    whether a target max inspiration is reached.

    o Pursed-lip breathing Lightly purse lips together during controlled exhalation Adopted spontaneously by patients with COPD to deal with episodes of dyspnea

    o Positive expiratory pressure breathing Resistance to airflow is applied during exhalation Similar to pursed-lip except that that patient breathes through a specially

    designed mouthpiece or mask that controls resistance to airflow.

    Used to hold airways open during exhalation to mobilize accumulated secretionsand improve their clearance.

    Respiratory muscle endurance training and helps to reduce fatigue. Airway clearance strategies are mandatory to reduce the work of breathing, improve gas

    exchange and limit infection. This is indicated for persons with

    o Abnormal cough mechanics Muscle weakness

    o Altered mucus rheology Cystic fibrosis

    o Structural airway defects Bronchiectasis

    o Altered mucociliary clearance Primary ciliary dyskinesia

    Techniques for clearing secretions includeo Postural drainage

    Aka bronchial drainage

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    Consists of positioning the patient according to bronchopulmonary anatomy sothat a particular lung segment is placed with its bronchus perpendicular togravity.

    Goal is to facilitate drainage of secretions into the segmental bronchus fromwhich they can be removed by coughing

    o Manual/device-induced airway oscillationo Chest percussion

    Rhythmically and alternately striking the chest wall over specific lung segmentswit cupped hands to mechanically jar and dislodged retained secretions

    PT molds his hands to fit the contour of the area being treated and applies a forcethat is appropriate t the individual patient

    Force is adjusted according to patent tolerance and should not be uncomfortablefor it is not the force but the cupping that is effective

    It should be continued for 2-5mins per lung segment then followed by vibrationand coughing or suctioning.

    o Vibration Consists of chest compression with manual vibration produced by tensing all

    muscles in the upper extremities in cocontraction.

    Performed during exhalation only, it aims at moving the mucous that wasdislodged during percussion toward the larger airways.

    PT hand placement can be on both sides of the patients chest or one hand on topof the other

    Patient takes a deep inspiration and then chest compression with vibration areperformed throughout exhalation for 6-8 breaths .

    o Shaking and rib springing Shaking is similar to vibration except that it consists of gentle thrusts in and out

    rather than vibrations with chest compression

    Rib springing is a more vigorous form of shaking in which the ribs are pumped ina springing fashion 3-4x during exhalation

    Contraindicated in patients with rigid chest walls, osteoporosis or other boneabnormalities.

    o Coughing Primary means of clearing airways of excess secretions and foreign material Either a reflex or voluntarily, an effective cough consists

    deep inspiration closure of the glottis with contraction of the abdominal muscles opening of the glottis with expulsion of the trapped air by forceful

    abdominal contraction

    impairment results in retained secretions and bronchial obstruction Teach patient the importance of an effective cough, how to produce an efficient

    and controlled voluntary cough and when to cough.

    For chest PT to be effective, mucoactive medications must be giveno Expectorantso Mucolyticso Bronchodilatorso Surfactantso Mucoregulatory agentso Antitussives for uncontrolled coughing

    Chest mobilization exercises

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    o Maintain and improve mobility of chest wall, trunk and shoulder girdle when it affectsventilation or postural alignment.

    o Combine stretching of hypomobile trunk muscles with deep breathing Exercise conditioning

    o A candidate must demonstrate a decrease in functional exercise capacity as a result of apulmonary disease and be able to participate safely in a rigorous cardiorespiratory

    endurance training program.o Cardiorespiratory exercise training is often effective for decreasing exertional dyspnea.o In patients with COPD, cardiorespiratory endurance exercise therapy has been shown to

    improve maximum or symptom-limited aerobic capacity, timed-walk distance and health-

    related quality of life. Adding resistance training to the rehabilitative program can

    provide additional benefits such as increased fat-free mass and muscle strength.

    o Several adjunct modalities might reduce the extreme breathlessness ad peripheral musclefatigue that prevent patients with severe COPD from exercising at higher intensities.

    Continuous positive airway pressure and NIPPV during exercise might reduce the perception ofdyspnea.

    Adding electrical stimulation to strength exercises for peripheral muscles has been shown tofurther improve muscle strength in patients with COPD.

    Oxygen supplementation, even in patients who dont desaturate during exercise allows for higherexercise intensities and produces a superior training effect.

    High intensity physical group training in water can produce significant benefits as well. Continuous outpatient exercise training, home-based or community-based exercise programs or

    exercise training in groups of persons with COPD is necessary to sustain the benefits acquired

    during the initial rehabilitation program.

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    Restrictive Lung Dysfunction

    Etiology

    Restrictive Lung Dysfunction (RLD) is an abnormal reduction in pulmonary ventilation.

    Lung expansion is diminished. The volume of air or gas moving in and out of the lungs is decreased. Pulmonary edema

    o Extravascular water in the lungs, usually caused by back pressure from failing left heart.o Main symptom: BREATHLESSNESS

    Pulmonary embolio Blockage of the pulmonary vasculature, usually by a blood clot

    Restrictive Lung Dysfunction is not a disease. In fact, this dysfunction may result from many

    different diseases arising from the pulmonary system or almost any other system in the body. It can

    also result from trauma or therapeutic interventions, such as radiation therapy or the use of certain

    drugs.

    Pathogenesis

    Three major aspects of pulmonary ventilation must be considered to understand the pathophysiology of

    RLD. They are compliance of both the lung and the chest wall, lung volumes and capacities, and the work

    of breathing.

    Compliance

    Physiologic link that establishes a relationship between the pressure exerted by the chest wall orthe lungs and the volume of air that can be contained within the lungs.

    With RLD chest wall or lung compliance, or both, is decreased.Lung Volumes

    Restrictive lung dysfunction eventually causes all the lung volumes and capacities to becomedecreased.

    Because the distensibility of the lung is decreased, the inspiratory reserve volume (IRV) isdiminished.

    Work of Breathing

    With RLD the work of breathing is increased.Clinical Manifestations

    6 Classic Signs

    1. Tachypnea or an increased respiratory rate. Early in the course of RLD there may beovercompensation, with the respiratory rate increasing to the point that minute ventilation is

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    increased and alveolar hyperventilation occurs, resulting in greater exhalation of carbon

    dioxide (CO2).

    2. Hypoxemia. A condition in which arterial oxygenation is below normal. Ventilation-perfusion mismatching, an invariable finding in RLD, leads to

    hypoxemia. This mismatching may be due to changes in the collagenous framework

    of the lung, scarring of capillary channels, distortion or narrowing of the small

    airways, compression from tumors within the lung or bony abnormalities of the chest

    wall, or a variety of other causes. Even if patients are not hypoxemic at rest, they may

    quickly become hypoxemic with exercise.

    3. Decreased breath sounds with dry inspiratory rales (Velcro cracles)4. Decrease in lung volumes and capacities5. Diffusing capacity (DLCO). This arises as a consequence of a widening of the interstitial

    spaces due to scar tissue, fibrosis of the capillaries, and ventilation-perfusion abnormalities.

    In RLD the DLCO has been measured at less than 50% of predicted.

    6. Cor Pulmonale. Right-sided heart failure is due to hypoxemia, fibrosis and compression ofthe pulmonary capillaries, which leads to pulmonary hypertension.

    Other signs:

    Decrease in chest wall expansion Possible cyanosis or clubbing

    3 Hallmark Symptoms

    1. Dyspnea2. Irritating, dry, non-productive cough.3. Wasted, emaciated appearance

    Signs and Symptoms of Restrictive Lung Dysfunction

    Signs Symptoms

    Tachypnea

    HypoxemiaDecreased lung volumes

    Decresed diffusing capacities

    Decrease breath soundsAltered chest radiograph (often reticulonodular

    pattern)

    Pulmonary hypertension

    Dyspnea

    CoughWeight loss

    Muscle wasting

    Differential Diagnosis

    In Restrictive Lung DiseaseForced expiratory volume in one second (FEV1) and forced vital capacity (FVC) are

    reduced so theFEV1/FVC ratio is normal.

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    In Obstructive Lung DiseaseFEV1 is reduced while the FVC is normal thus the FEV1/FVC ratio is lower.

    Medical Management

    1. Supplemental Oxygen to support the arterial partial pressure2. Antibiotic therapy to fight secondary pulmonary infection3. Measures to promote adequate ventilation and prevent accumulation of pulmonary secretions4. Good nutritional support

    However, if the changes that are causing the RDL are acute and reversible (pneumothorax) or chronic but

    reversible (Guillain-Barre syndrome), the treatment consists of specific corrective interventions (e.g.,

    chest tube placement) as well as supportive measures (e.g., temporary mechanical ventilation) to assist the

    patient to maintain adequate ventilation until the patient is again able to be independent in this activity.

    RLD Management Goals

    1. Improve exercise tolerance of the patient

    2. Increase/bring back to normal lung volume of patient

    3. Decrease/bring back to normal patients work of breathing4. Bring relief of pain, anxiety or tension, fatigue

    Physical Therapy Management

    1. Treatment program that includes:

    Low-level activity initially with gradual progression Periodic rest periods to increase patient tolerance of more vigorous activities Coordination of breathing with activity Techniques to increase pulmonary compliance

    o Breathing exerciseso Thoracic mobility and posture exerciseso Soft tissue mobilization

    Bronchial hygiene techniques if secretion management is a problemo Postural Drainage with percussion and/or vibration (PD&P) (PD&V)o High Frequency Compression/Oscillation Therapyo Flutter Valveo IntraPulmonary Percussive Ventilationo Positive Airway Pressure Techniqueso Positive Expiratory Pressure Therapy (PEP)

    Relaxation techniques2. Aerobic or endurance training

    Exercise involving large muscles of the body, which is sustained continuously for at least 20 to30 minutes at an intensity of 70% to 85% of maximal predicted heart rate (according to age) and

    performed at least 3 days per week

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    3. Breathing pattern control

    Teach patients specific breathing strategies including diaphragmatic breathing, pursed-lipbreathing to reduce work of breathing by slowing the respiratory rate or eliminating accessorymuscle activity, especially during exertion.

    4. Positioning

    Lung compliance decreases and work of breathing increases progressively from standing, tositting, to supine. In supine, lung volume is restricted by the load of the viscera, increasedthoracic blood volume, and small airway closure.

    No physiotherapy should be carried out without consideration of the position in which it isperformed.

    5. Deep breathing

    Accurately position patient, usually side-lying-inclined-towards-prone to facilitate maximumexpansion of the base of the uppermost lung

    If side-lying is impossible, upright sitting may be done When patient is ready, he/she is asked to breathe in deeply and slowly through the nose, then sigh

    out through the mouth

    After every few breaths, patient should relax and regain his/her rhythm Breathing rate and pattern should be observed at this time

    6. AROM exercises strengthening exercises, bracing

    Required for patients with paralysis7. Teach patients to increase and strengthen endurance of remaining ventilator muscles by:

    Use of an inspiratory muscle trainer Resistance exercise to the diaphragm Incentive spirometer

    8. Patient must learn to perform: Active and passive chest wall stretching (rolling, positioning, side leaning, air shift maneuvers)

    9. PROM may be done immediately

    Sources:

    Braddom, R.L. (2011). Physical Medicine & Rehabilitation. 4th

    ed. Singapore: Elsevier Pte. Ltd.

    Hillegas, A. & Sadowsky, H. (2001). Essentials of Cardiopulmonary Physica Therapy. 2nd ed. USA: W.B.

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